Increase In Plasma Epinephrine Concentration Research Articles

Sustained increases in plasma epinephrine concentration do not modulate renin release

We examined the relationship between plasma renin activity (PRA) and renal arterial pressure (RAP) during 1) control conditions, 2) acute, and 3) chronic intravenous epinephrine (EPI) infusion (125 ng.kg-1.min-1). In eight conscious uninephrectomized dogs maintained on a normal sodium intake, the renin stimulus-response curve (RSRC) was determined by a stepwise reduction in RAP with an inflatable occluder around the renal artery controlled by a servo unit. The RSRC could be approximated by two lines intersecting at a threshold pressure (approximately 20 mmHg below control RAP). In the high-pressure range, PRA was relatively insensitive to changes in RAP, whereas, below threshold pressure, changes in RAP had large effects on PRA. During acute EPI infusion there was approximately a 40% increase in heart rate (control = 57 +/- 3 beats/min) and hematocrit (control = 30 +/- 1%) in association with a rise in plasma EPI concentration from 73 +/- 16 to 1,413 +/- 100 pg/ml; mean arterial pressure (MAP) was unchanged (94 +/- 3 mmHg). Moreover, EPI acutely increased basal PRA from 0.3 +/- 0.1 to 0.8 +/- 0.3 ng angiotensin I.ml-1.h-1 and shifted the RSRC to the right (increasing threshold pressure 7 mmHg) without altering the slope of the RSRC curve either above or below threshold pressure. In contrast, although plasma EPI concentration and hematocrit remained elevated during chronic EPI infusion, heart rate and basal PRA returned to preinfusion values. In addition, there were no significant long-term changes in MAP or in any of the parameters of the RSRC.(ABSTRACT TRUNCATED AT 250 WORDS)

Why does vasodilatation occur during syncope?

1. Syncopal or near syncopal episodes have been observed in five subjects who stood or were tilted and in whom blood samples were being taken. 2. In all subjects bradycardia and hypotension developed before the onset of symptoms. Increases in plasma adrenaline concentrations occurred in all subjects, beginning before the faint. Changes in plasma noradrenaline concentrations were variable: in three subjects there was a marked fall and in the other two subjects an increase. Plasma vasopressin increased in all subjects. 3. Increase in plasma adrenaline may be contributing to the vasodilatation and arterial hypotension which occur during syncope.

Effects of epinephrine on branchial and renal calcium handling in the rainbow trout.

Acute exposure of rainbow trout (Salmo gairdneri) to low external calcium (25 microM) caused an immediate but transient increase in plasma epinephrine concentration that may have been related to a concomitant depression of blood pH. Intra-arterial infusion of epinephrine at normal ambient calcium levels (0.35 mM) for 4 h caused circulating levels of epinephrine to rise from 2.9 X 10(-9) to 8.0 X 10(-8) M but did not affect norepinephrine levels, or branchial unidirectional calcium fluxes. Active (ATP-dependent) calcium transport across basolateral plasma membranes prepared from gill epithelial cells was not affected by pretreatment of fish with epinephrine or by direct application of epinephrine or cAMP, in vitro. Epinephrine infusion elevated urine flow rate, decreased urine pH, and increased urine phosphate levels significantly. Net renal calcium efflux increased significantly as a result of the increased urine flow rate. It is concluded that epinephrine does not stimulate branchial calcium uptake or renal conservation of calcium in rainbow trout at normal external calcium levels and therefore we cautiously suggest that epinephrine is unlikely to be involved in calcium balance during periods of exposure to low external calcium. Instead, epinephrine may play a role in compensating the acid-base disturbances and the increased branchial water influx that are associated with exposure to low ambient calcium.

Adrenomedullary origin of the hindquarter vasodilation during the transposition response of the rat.

Transposing a rat from the home cage to a new cage produces a cardiovascular response (transposition response) characterized by an increase in hindquarter blood flow with unchanged systemic arterial pressure. Arterial blood samples were collected from rats before and during this response for radioenzymatic assay of catecholamines. During the transposition response, the concentration of adrenaline and noradrenaline in plasma increased about six- and two-fold, respectively. Ablation of the adrenal medulla prevented these changes in plasma catecholamine concentration. Constant i.v. infusion of adrenaline, at rates producing a hindquarter flow approximately matching that observed during the transposition response, evoked an increase in plasma adrenaline concentration also approximately matching the increase observed during the transposition response. It is concluded that the increase in plasma adrenaline secreted from the adrenal medulla is the main cause of the increase in hindquarter blood flow in the transposition response.

Homeostatic regulation of airway smooth muscle tone by catecholamine secretion in swine.

We studied the homeostatic secretory response of catecholamine secretion elicited by progressive bronchoconstriction in 18 swine in vivo. The potential reserve of the sympathetic nervous system (SNS) was first assessed by exogenous nicotinic stimulation with 1,1-dimethyl-4-phenylpiperazinium iodide (DMPP). A dose of 250 micrograms/kg iv DMPP caused an increase in plasma norepinephrine (NE) concentration from 207 +/- 86 (basal) to 2,625 +/- 448 pg/ml (P less than 0.02) and in plasma epinephrine (EPI) from 10 +/- 5.0 to 1,410 +/- 432 pg/ml (P less than 0.05) in four swine. In four other swine, bronchoconstriction induced by aerosolized prostaglandin F2 alpha caused approximately a fivefold increase in airway resistance without hemodynamic changes. No increase in plasma EPI was observed. However, plasma NE increased from 330 +/- 131 to 1,540 +/- 182 pg/ml (P less than 0.02). In five swine receiving aerosolized acetylcholine (ACh), similar changes in airways resistance were not associated with significant changes in catecholamine concentration when mean arterial blood pressure (MAP) was unchanged. However, inhalation of sufficient ACh to cause a greater than 10% decrease in MAP caused progressive increase in catecholamine secretion. Plasma EPI increased from 32 +/- 16 (MAP = 124 +/- 7 Torr) to 1,165 +/- 522 pg/ml (MAP = 94 +/- Torr). Hypoxemia that occurred with bronchoconstriction (greater than or equal to 50 Torr) did not cause catecholamine secretion. However, severe hypoxemia (PO2 less than 30 Torr) caused large increases in plasma EPI concentrations from 84 +/- 27 to 1,463 +/- 945 pg/ml (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiovascular Actions of Nitrous Oxide or Halothane in Hypovolemic Swine

During normovolemia, nitrous oxide causes mild sympathetic stimulation and direct myocardial depression; these effects offset each other, resulting in only minimal cardiovascular changes. To test the hypothesis that during hypovolemia this balance would change and depression predominate, 10 swine were made hypovolemic (30% blood loss) and then were given 70% N2O (0.25 MAC in swine) or an equipotent concentration of halothane, an agent that does not cause sympathetic stimulation. The alternate anesthetic was given to the same hypovolemic swine on another day. Five minutes after induction of anesthesia during hypovolemia, both N2O and halothane caused significant, physiologically important deterioration of compensation for hemorrhage. Halothane decreased systemic vascular resistance (SVR); N2O was more variable in its action, and SVR did not decrease significantly. Both agents caused similar decreases in cardiac output, mean aortic blood pressure, stroke volume, oxygen consumption, and left ventricular minute work, despite increases in plasma epinephrine concentration and plasma renin activity. No differences were found between groups for any of these variables (P greater than 0.05). Plasma norepinephrine concentration increased only in the N2O group and was greater in that group than in the halothane group. The deterioration of cardiovascular compensation for hemorrhage was expressed metabolically by similar decreases in the two groups in partial pressure of oxygen of mixed venous blood and by increases in blood lactate concentration. Thirty minutes after induction of anesthesia, with stable end-tidal anesthetic concentrations, both groups had some cardiovascular, but no metabolic, recovery.(ABSTRACT TRUNCATED AT 250 WORDS)

CHANGES IN PLASMA CATECHOLAMINE CONCENTRATIONS FOLLOWING INFILTRATION WITH LARGE VOLUMES OF LOCAL ANAESTHETIC SOLUTION CONTAINING ADRENALINE

Plasma catecholamine concentrations have been measured in nine patients undergoing rhinoplasty following infiltration to the facial area of 21 ml of 0.5% lignocaine with adrenaline 1:200,000 and in seven patients undergoing brachial plexus blockade with 40 ml of 0.5% lignocaine, 0.25% bupivacaine and adrenaline 1:200,000. In the rhinoplasty group there was a 566% increase in plasma adrenaline concentration 2 min after cessation of infiltration, whilst in the brachial plexus group a 112% increase in the plasma concentration of adrenaline occurred at 10 min after completion of the block. There was no change in plasma noradrenaline concentration in either group. It is concluded that the so-called safe dose of adrenaline (1.0 microgram kg-1 during halothane anaesthesia) is meaningless unless the site of administration is specified.

MEASUREMENT OF PLASMA CATECHOLAMINE CONCENTRATIONS: An Assessment of Anxiety

This study was designed to assess the value of measurement of plasma catecholamine concentrations as an objective index of anxiety. A preliminary study was undertaken on 11 healthy volunteers (medically qualified), to determine if venous cannulation per se produced any change in plasma catecholamine concentrations. There were no changes in plasma catecholamine concentrations in the 2 h following insertion of an i.v. cannula, suggesting that venous cannulation did not induce a measurable stress response. A second study was performed on 48 surgical patients who were asked to rate their perceived anxiety on a linear analogue scale immediately before premedication and immediately before induction of anaesthesia. Venous blood was obtained at the same time as these ratings. There were no significant changes in perceived anxiety or plasma noradrenaline concentrations following premedication. However, compared with values before premedication, there was a mean percentage increase in plasma adrenaline concentration of 40% before induction of anaesthesia. A significant correlation was shown between mean percentage change in Linear Analogue Anxiety Score and mean percentage change in plasma adrenaline concentrations (r = 0.32).

Plasma, Adrenal, and Heart Catecholamines in Physically Trained Normal and Diabetic Rats

This study was designed to evaluate the possibility that the enhanced insulin sensitivity of physically trained normal and diabetic rats is due to adaptive changes in the adrenergic system. Mild diabetes mellitus was induced in male Wistar rats with streptozocin (STZ, 45 mg/kg i.v.) and a 10-wk conditioning program was conducted by having the animals run on a treadmill. Rats were cannulated 16 h after the last period of exercise and blood sampling was obtained 48 h later for basal plasma glucose, insulin, epinephrine, and norepinephrine determination. Catecholamine measurements were also made in adrenals, atria, and ventricles from sedentary control, trained control, sedentary diabetic, and trained diabetic rats. The previously reported beneficial effect of physical training on diabetes mellitus was reproduced. While diabetes mellitus did not modify the catecholamine levels, the training program provoked an increase in plasma epinephrine concentrations, with a concomitant significant rise in adrenal epinephrine content. In heart tissue, the epinephrine values also tended to be increased by training although statistical significance was not reached. These data suggest that basal secretion of epinephrine is somewhat increased in trained rats. Whether this may trigger adaptive changes that could be involved in the beneficial effect of physical training on experimental diabetes mellitus remains to be elucidated.

Adrenomedullary response to maximal stress in humans

The most important neuroendocrine response to stress is an increase in plasma epinephrine concentration. To investigate the clinical significance of this response, plasma catecholamine levels were measured (single-isotope derivative assay) in chronic stress (severe illness; n = 22) and acute maximal stress (cardiac arrest; n = 23). The results were then compared with the values from 60 normal resting subjects: epinephrine (mean ± SEM) 0.034 ± 0.002 ng/ml; norepinephrine 0.228 ± 0.01 ng/ml. Chronic stress (intensive care unit patients) was associated with a fourfold elevation of epinephrine concentration (0.14 ± 0.06 ng/ml; range 0.01 to 1.37; p < 0.01 versus normal control subjects). Acute maximal stress (resuscitation following cardiac arrest) resulted in a greater than 300-fold increase in the plasma epinephrine level (10.3 ± 2.9 ng/ml; range 0.36 to 35.9; n = 15; p < 0.01). Peak plasma epinephrine levels in successfully resuscitated patients (n = 6) ranged from 0.36 to 273 ng/ml (three patients had received epinephrine therapy). The plasma norepinephrine level was increased twofold in intensive care unit patients (0.52 ± 0.06 ng/ml; p < 0.01) and 32-fold after cardiac arrest (7.37 ± 1.8 ng/ml; p < 0.01). During resuscitation, the correlation between the simultaneous epinephrine and norepinephrine levels was highly significant: r = 0.76; p < 0.01. It is concluded that (1) chronic, severe stress produces only moderate elevations of plasma epinephrine levels (up to 1.37 ng/ml), whereas acute stress produces marked increases of plasma epinephrine that may reach the extraordinarily high level of 35.9 ng/ml, (2) the potential toxicity from the adrenomedullary response to acute stress is further exacerbated by the parallel release of norepinephrine, and (3) under close medical monitoring, it is possible to survive with plasma epinephrine concentrations as high as 273 ng/ml.

Vascular recovery following hemorrhage in the dogfish shark Squalus acanthias.

Cardiovascular regulatory systems were examined in the dogfish shark after hemorrhage of 1% of body weight. An immediate 45% decrease in mean dorsal aortic pressure and delayed increases in plasma epinephrine concentration and plasma norepinephrine concentration were noted. During the recovery period following hemorrhage, the catecholamine levels peaked (epinephrine 203% of control, norepinephrine 148% of control) and then returned toward control values. Hematocrit, however, continued to decline as blood pressure recovered. Phentolamine pretreatment, which in itself caused a 55% decrease in dorsal aortic pressure, did not prevent the recovery of blood pressure after hemorrhage. This study indicates that 1) hemorrhage causes an increase in circulatory catecholamine concentration, possibly by a baroreceptor reflex; 2) volume recruitment, as indicated by the drop in hematocrit, is a major mechanism contributing to the recovery of dorsal aortic pressure after hypotension; and 3) alpha-adrenergic receptors are not necessary for the recovery of dorsal aortic pressure after hemorrhage.

Gonadotropin-releasing hormone increases plasma catecholamines and blood pressure in toads.

Synthetic gonadotropin-releasing hormone (GnRH) was injected intravenously into conscious, adult toads (Bufo marinus) to elucidate the nervous and cardiovascular actions of the hormone. GnRH (0.001-1.0 nmol X kg-1) produced dose-dependent increases in mean arterial blood pressure and pulse pressure, beginning within 3 min after injection. These pressor responses to GnRH were specific to the hormone since they could be inhibited reversibly by [D-pGlu1, D-Phe2, D-Trp3,6]-GnRH. Arterial plasma concentrations of unconjugated catecholamines increased simultaneously with the rise in blood pressure following GnRH injection: the half-maximal pressor dose of GnRH (0.1 nmol X kg-1) caused a 3-fold increase in plasma noradrenaline and a 20-fold increase in plasma adrenaline concentrations. Pretreatment of toads with an alpha-adrenergic antagonist, prazosin, and a beta-adrenergic antagonist, propranolol, abolished the pressor responses to GnRH. We conclude that GnRH mobilizes catecholamines, which act through alpha- and beta-adrenergic mechanisms to raise blood pressure. Thus, endogenous GnRH or GnRH-like peptides may coordinate the pituitary, nervous and cardiovascular mechanisms which prepare toads for seasonal reproductive activity.

Responses of plasma catecholamine and plasma renin activity after glucagon stimulation in essential hypertension.

Abstract. To investigate the roles of the sympatheticoadrenomedullary system and the renin-angiotensin system in the pathogenesis of essential hypertension, the levels of plasma catecholamine and plasma renin activity (PRA) after glucagon-stimulation were evaluated. In 9 patients with essential hypertension whose levels of PRA were either normal or high (NHREH), iv bolus injection of 1 mg glucagon caused a rapid and significant increase in plasma epinephrine concentration from the basal values of 170 ± 25 pg/ml, mean ± sem to 314 ± 30 pg/ml (P &lt; 0.05) at 5 min after the injection, reaching the mean peak values of 358 ± 87 pg/ml (P &lt; 0.05). Plasma norepinephrine also rose from the basal values of 357 ± 50 pg/ml to the peak values of 1065 ± 231 pg/ml (P &lt; 0.02) while increase in PRA was detected in 4 of 9 patients. In 7 patients with low renin essential hypertension (LREH), plasma epinephrine failed to increase after glucagon stimulation whereas plasma norepinephrine increased significantly from the basal values of 391 ± 77 pg/ml, reaching 1212 ± 274 pg/ml at their peak values (P &lt; 0.01). There was no discernible response of PRA to glucagon. These results suggest that both epinephrine secretion from adrenal medulla and renin release from juxtaglomerular (JG) cells after glucagon injection are impaired in LREH in contrast to their significant responses observed in NHREH. It also indicates that glucagon load may be useful for the simultaneous assessment of the reserve of both renin secretion and sympatheticoadrenomedullary function in essential hypertension.

Interrelationships between urea, ammonia, glucose, insulin and adrenaline during ammonia-urea toxicosis in sheep ( Ovis aries)

1. 1. The effects of intra-ruminal administration of urea on plasma urea, ammonia, glucose, insulin and adrenaline concentrations and the response pattern of glucose to exogenous insulin were studied in sheep. 2. 2. Urea toxicosis was associated with hyperglycemia, hypoinsulinemia and a profound increase in plasma adrenaline concentration. 3. 3. Mechanisms involved in glucose metabolism in ruminants in relation to glucose production rate are discussed.

Central cardiovascular effects of prostacyclin

The central cardiovascular effects of prostacyclin (PGI 2) were studied in rats anesthetized with halothane. Prostacyclin (5–5000 ng/300 g) was injected intravenously, intracerebroventricularly (i.c.v.) and into discrete hypothalamic nuclei (50 ng/300 g). Injection of prostacyclin intracerebroventricularly showed a dose-dependent vasodepressor and cardiac-accelerating effect; however the intracerebroventricular responses were less potent than those obtained with intravenous administration of prostacyclin. Injection of prostacyclin into the dorsomedial nucleus of the hypothalamus elicited tachycardia and a moderate increase in plasma epinephrine concentration, without any change in the systemic blood pressure. The cardiac-accelerating response obtained by injection of PGI 2 into the dorsomedial nucleus was not abolished by acute bilateral adrenalectomy. It is concluded that cardiovascular responses obtained by intracerebroventricular injections of PGI 2 probably represent peripheral effects of this prostaglandin. Injections into discrete brain nuclei may provide better information as to the central effects of prostacyclin. The present report suggests that PGI 2 modulates heart rate by an action in the region of the dorsomedial nucleus of the hypothalamus.

Evaluation of plasma norepinephrine as an index of sympathetic neuron function in the conscious, unrestrained rat

Measurement of plasma norepinephrine and epinephrine concentrations in the conscious, unrestrained rat yielded values of 138±10 and 55±8 pg/ml, respectively. Ganglionic blockade reduced basal norepinephrine levels without affecting plasma epinephrine levels. Adrenal demedullation reduced plasma epinephrine to undetectable levels (<20 pg/ml) and gave rise to an apparent compensatory increase in plasma norepinephrine levels. Adrenal demedullation in combination with ganglionic blockade reduced plasma norepinephrine to the same level as did ganglionic blockade alone. These observations indicated that the plasma epinephrine was of adrenal origin. Furthermore, under these experimental conditions, the results suggested that the major portion of the plasma norepinephrine was of neuronal origin. When specific destruction of the sympathetic nerve terminals without alteration of adrenal medullary function was accomplished with 6-hydroxydopamine, a fivefold increase in plasma epinephrine concentration was observed at 24 hours. Plasma norepinephrine levels at 24 hours were not significantly altered from the control levels by the 6-hydroxydopamine suggesting that the rodent adrenal medulla was capable of secreting substantial amounts of norepinephrine under these conditions. It was concluded that plasma norepinephrine concentrations reflect both sympathetic neuronal and adrenomedullary activity. However, in the absence of changes in plasma epinephrine, plasma norepinephrine appears to be an index of sympathetic neuron function.